FGL2 improves experimental colitis related to gut microbiota structure and bile acid metabolism by regulating macrophage autophagy and apoptosis.

ABSTRACT: Inflammatory bowel disease (IBD) is a refractory disease with immune abnormalities and pathological changes. Intestinal macrophages are considered to be the main factor in establishing and maintaining intestinal homeostasis. The immunoregulatory and anti-inflammatory activity of fibrinogen-like protein 2 (FGL2) can regulate macrophage polarization. However, its function in IBD is unclear. In this study, we explored the effect of FGL2 on macrophage polarization, autophagy, and apoptosis in bone marrow-derived macrophages (BMDMs) treated with lipopolysaccharide (LPS) and further investigated changes in the intestinal barrier, flora, and bile acid in dextran sodium sulfate (DSS)-treated mice. Our results demonstrated that FGL2^-/- weakened ERK signaling to promote M1 polarization an

SUBMITTER: Zhao Y 

PROVIDER: S-EPMC11298944 | biostudies-literature | 2024 Jul

REPOSITORIES: biostudies-literature